In addition to increased fructose consumption being a risk factor for NAFLD, fructose has been implicated in NAFLD disease progression. The administration of a diet with 25% of total energy as sucrose (which contains 50% fructose) resulted in a rise in liver aminotransferase levels within 18 days. This study, performed nearly 25 years ago, is all the more alarming as current sugar intake of Americans is in this same range. In our study of 427 patients with biopsy-proven NAFLD, increased consumption of fructose-containing beverages was univariately associated with decreased age (P < 0.0001), male sex (P < 0.0001), hypertriglyceridemia (P < 0.04), low high density lipoprotein (HDL) cholesterol (<0.0001), decreased serum glucose (P < 0.001), increased calorie intake (P < 0.0001), and hyperuricemia (P < 0.0001). After controlling for age, sex, BMI, and total calorie intake, daily fructose consumption was associated with lower steatosis grade and higher fibrosis stage (P < 0.05 for each). Being that triglyceride synthesis requires ATP, we hypothesize that lower hepatic steatosis may reflect deceased ATP availability. Additionally, in older adults (age ≥ 48 years), daily fructose consumption was associated with increased hepatic inflammation (P < 0.05), and hepatocyte ballooning (P< 0.05). However, the mechanism(s) by which fructose causes liver injury remains unknown.